Cornett J B
J Virol. 1974 Feb;13(2):312-21. doi: 10.1128/JVI.13.2.312-321.1974.
Cells of Escherichia coli B infected with the immunity-negative (imm2) mutant of bacteriophage T4 are able to develop a substantial level of immunity to superinfecting phage ghosts if the ghost challenge is made late in infection. This background immunity is not seen in infections with phage carrying the spackle (s) mutation in addition to the imm2 lesion. The level of immunity in s(-) infections is intermediate between that of imm(-) and wild-type infections under standard assay conditions. With respect to genetic exclusion of superinfecting phage, cells infected with imm(-) phage are completely deficient, whereas infections with the s(-) phage are only partially deficient compared to wild-type infections. Whereas s(-)-infected cells are unable to resist lysis from without by a high multiplicity of infection (MOI) of superinfecting phage, cells infected with imm(-) phage show less than wild-type levels of resistance and the majority of cells remaining intact are unable to incorporate leucine or form infective centers. Under conditions of superinfection by low MOI of homologous phage, imm(-)-infected cells are lysis inhibited, whereas s(-)-infected cells do not show this property. Superinfecting phage inject their DNA into imm(-)-infected cells with the same efficiency as seen in wild-type infections, but this efficiency is reduced when the cells are first infected with s(-) phage. The s function of T4 appears not only to affect the host cell wall as previously postulated by Emrich, but may also affect the junctures of cell wall and membrane with consequences similar to those of the imm function.
用噬菌体T4的免疫阴性(imm2)突变体感染的大肠杆菌B细胞,如果在感染后期受到噬菌体幽灵的挑战,能够产生相当程度的对超级感染噬菌体幽灵的免疫力。如果除了imm2损伤外还携带斑点(s)突变的噬菌体感染,则看不到这种背景免疫力。在标准检测条件下,s(-)感染中的免疫水平介于imm(-)和野生型感染之间。关于超级感染噬菌体的遗传排斥,感染imm(-)噬菌体的细胞完全缺乏,而与野生型感染相比,感染s(-)噬菌体的细胞只是部分缺乏。虽然感染s(-)的细胞不能抵抗高感染复数(MOI)的超级感染噬菌体的体外裂解,但感染imm(-)噬菌体的细胞显示出低于野生型水平的抗性,并且大多数保持完整的细胞不能掺入亮氨酸或形成感染中心。在同源噬菌体低MOI超级感染的条件下,感染imm(-)的细胞的裂解受到抑制,而感染s(-)的细胞则没有这种特性。超级感染噬菌体将其DNA注入感染imm(-)的细胞的效率与野生型感染中所见相同,但当细胞首先感染s(-)噬菌体时,这种效率会降低。T4的s功能似乎不仅如Emrich先前假设的那样影响宿主细胞壁,而且可能还影响细胞壁和细胞膜的连接点,其后果与imm功能类似。